Barley (1,3)-β-d-Glucan Dietary Supplementation Prevents Cardiac Dysfunction in Obese Mice with Psychosocial Stress by Attenuating Myocardial Oxidative Stress

Objective: Obesity due to high fat intake and psychosocial stress (PSS) are major determinants of cardiovascular disease (CVD), particularly when combined. Long-term diets enriched with barley (1,3)-β- d-glucan (BBG), an inhibitor of the class I histone deacetylases and an antioxidant, increases post-ischemic survival rate in mice by promoting angiogenesis. However, the impact of a BBG-enriched diet on cardiac dysfunction due to conditions such as high-fat diet (HFD) and PSS, alone or in combination, is unknown. Here, we tested whether supplementing HFD-treated mice with BBG prevents HFD- or HFD/PSS induced cardiac dysfunction by attenuating myocardial oxidative stress. Methods: Controlmale C57BL/6 mice were fed with 3 different diets for 18 wks: 1) standard diet (SD; 10% kcal fromfat; n=9); 2) HFD (58%kcal from fat; n=9); or 3)HFD+3% BBG (HFD+BBG; 58% kcal from fat; n = 9). All mice were then subjected chronic PSS via a daily (10min) encounter with a male intruder (resident/intruder test, fromweek 16 to week 18). Cardiac function was evaluated by echocardiography before and after PSS, whereas left ventricle (LV) tissue was collected at study termination to assess reactive oxygen species (ROS) by emission electron paramagnetic resonance analysis. Results: At week 16, body weight was markedly higher in the HFD than in the SD group (+60.1%, P < 0.001); however, BBG supplementation significantly prevented weight gain (−10% compared with HFD, P < 0.05). The addition of PSS significantly worsened the LV dysfunction in HFD (LV ejection fraction (LVEF), −25%; LV fractional shortening (LVFS), −33% compared with SD (LVEF, −7%; LVFS, −10%) mice. Conversely, the LV function after PSS was significantly improved in HFD + BBG mice (LVEF, +7%; LVFS, +10%) when compared with basal values. HFD and PSS led a marked rise in LV ROS production, as compared with values found in the hearts of mice receiving SD (+76% P < 0.001). However, this increment was significantly attenuated in HFD + BBG mice in which LV ROS emission rose only by 34%. Our study shows that a regular supplementation of 3% wt/vol BBG with diet prevents cardiac functional decay due to the combination of HFD and PSS, likely by countering HFD/PSS-induced myocardial ROS production. These findings may have preventative or therapeutic implications for all CVDs characterized by a cardiac, vascular, or both redox milieu.